inhibitors of protein synthesis II Flashcards

1
Q

prototype aminoglycoside

A

streptomycin

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2
Q

route of administration of streptomycin

A

IV; IM

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3
Q

List the aminoglycosides

A
  1. Streptomycin
  2. Gentamicin
  3. Tobramycin
  4. Amikacin
  5. Neomycin
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4
Q

route of administration of Gentamicin

A
  • IV
  • IM
  • topical
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5
Q

route of administration of Tobramycin

A
  • IV
  • IM
  • topical
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6
Q

route of administration of amikacin

A
  • IV
  • IM
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7
Q

route of administration of Neomycin

A
  • oral
  • topical
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8
Q

why is structure of aminoglycosides significant to their function

A
  • aminoglycosides are polar and very large
  • need to be actively transported (oxygen requiring process)
  • under aerobic conditions, aminoglycoside are bactericidal
  • NOT effective against anaerobic species
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9
Q

MOA of aminoglycoside

A
  • irreversibly inhibit protein synthesis
  • bind to 30S
  • bactericidal
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10
Q

coverage of aminoglycoside

A
  • aerobic G - enteric bacteria
  • suspicion of sepsis or endocarditis
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11
Q

DOC for enterococcus species

A

aminoglycoside + penicillin

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12
Q

DOC tularemia (rabbit hunting disease)

A

Gentamicin

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13
Q

DOC pseudomonas aeruginosa

A

aminoglycoside + antipseud. pencillin

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14
Q

aminoglycosides are time or concentration dependent killers

A

concentration dependent killing

  • increasing concentrations kill an increasing population os bacteria and at a more rapid rate
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15
Q

aminoglycoside have a significant post-antibiotic effect. What does this mean?

A
  • antibacterial activity persists beyond the time that the abx is measurable
  • single, large does has better efficacy than multiple smaller doses (reduces the toxic side effects)
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16
Q

aminoglycoside toxicity

A
  • ototoxicity
  • nephrotoxicity
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17
Q

why is it bad if a bacteria acquires resistance to one aminoglycoside

A
  • cross resistance
    • may exhibit cross resistance to the other aminoglycosides
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18
Q

are aminoglycosides mostly used alone to treat infections?

A

No, they are mostly used in combination with other abx

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19
Q

coverage of Chloramphenicol (chloromycetin)

A

broad spectrum antibiotic

  • not first choice-reserved to life threatening infections
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20
Q

toxicity of Chloramphenicol (chloromycetin)

A
  • dose-dependent
    • fatal aplastic anemia
    • bone marrow suppression
    • “Gray baby” syndrome
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21
Q

MOA of Chloramphenicol (chloromycetin)

A
  • reversibly binds the 50S subunit
  • protein synthesis is inhibited
  • bacteriostatic
22
Q

adverse effect of MOA of Chloramphenicol (chloromycetin)

A

can inhibit mitochondrial protein synthesis in mammalian cells

23
Q

route of administration of Chloramphenicol (chloromycetin)

A

Parenteral

24
Q

distribution of Chloramphenicol (chloromycetin) in the body

A
  • distributed widely in the body including eyes and CNS
    • ​BEST CNS penetration
25
Q

metabolism of Chloramphenicol (chloromycetin)

A

metabolized in the liver; conjugated with glucuronic acid

*has to be conjugated to be eliminated

26
Q

“gray baby” syndrome is associated with Abx

A

Chloramphenicol (chloromycetin)

  • inadequate activity of glucuronyl transferase in the newborn liver
  • inability to conjugate the Abx
27
Q

how do bacteria become resistant to Chloramphenicol (chloromycetin)

A

produce acetyl transferase which acetylates and inactivates Chloramphenicol

28
Q

What are the three Tetracyclines

A
  1. Tetracycline
  2. Doxycycline
  3. Minocycline
29
Q

what is the prototype tetracycline

A

tetracycline (Sumycin)

30
Q

route of administration of tetracycline (sumycin)

A
  • oral
  • topical
31
Q

route of administration of Doxycycline

A

oral

32
Q

route of administration of minocycline

A

oral

33
Q

MOA of tetracyclines

A
  • inhibition of bacterial protein synthesis
  • bacteriostatic
  • bind reversibly to 30S ribosomes
34
Q

coverage of tetracyclines

A

broad spectrum

35
Q

DOC Cholera

A

Doxycycline

36
Q

DOC Mycoplasma pneumonia

A

tetracyclines + erythromycin

37
Q

DOC infections with chlamydia

A

tetracyclines + azithro/erythro

38
Q

DOC Rickettsial infections

A

tetracyclines

39
Q

Early, localized Borrelia Burgdorferi infection (lyme disease)

A

Doxycycline

40
Q

DOC Vibrio species

A

tetracyclines

41
Q

tetracycline chelate with what metals

A
  • calcium
  • iron (Fe2+)
  • aluminum (Al3+)
42
Q

deposition of tetracycline

A

deposit in bone and teeth (chelate Ca2+)

43
Q

route of administration of tetracycline

A

oral is adequate but incomplete

44
Q

adverse reactions of tetracyclines

A
  • normal flora changes
  • bone (inhibit bone elongation) and Teeth (dental discoloration)
  • photosensitivity
45
Q

who should not be given tetracyclines

A
  • pregnant women
    • can cross placenta and is excreted in breast milk
  • children below the age of 8 years old
46
Q

What is the only Glycylcycline

A

Tigecycline (tigacil)

47
Q

MOA of Tigecycline

A
  • binds to 30S
  • bacteriostatic
48
Q

coverage of Tigecycline

A
  • similar to that of tetracycline, doxycycline, minocycline but shows activity against tetracycline-resistant organisms
49
Q

what specific organisms does Tigecycline cover

A
  • MRSA
  • MRSE (staph epidermidis)
  • PRSP (PCN-resistant strep pneumoniae)
  • VRE (vancomycin-resistant enterococci)
50
Q

what are the longer acting tetracyclines

A
  • Doxycycline and Minocycline
    • slowly excreted
    • have longer plasma half-life and require less frequent administration